Recent studies demonstrate that the inhibition of BCRABL TK task induces differentiation and apoptosis. In this study, however, the amount of Bcl 2 protein in K562 cell line did not change after experience of Pivanex. This could be because of the low basal levels of the protein. Inspite of the high basal levels of Bcl xL in K562 cells, Pivanex had no influence on the levels of the protein. Since Pivanex induces apoptosis, we conclude that unlike in HL 60 cells, this indicates that apoptosis induced by Pivanex in K562 cells doesn’t require natural product libraries these apoptotic regulating proteins. The process by which apoptosis is induced by Pivanex still must be examined. CML patients are now being treated with the encouraging drug Imatinib but existence of STI571 resistance and paid down responsiveness to STI571 in accelerated cycle of CMLor blast crisis have resulted in the look for novel drugs and other methods. It was found that exposure of K562 to HDI such as suberoylanilide hydroxamic acid, was minimally hazardous alone, and triggered a marked escalation in caspase activation, mitochondrial damage and apoptosis. Similar effects were obtained when STI571 and sodium butyrate were mixed. Pivanex, a butyric acid expert drug that is more potent than BA in inducing cell differentiation, inhibition of cell growth gene expression and hyperacetylation in cell cultures and in vivo, was opted for as a potent HDI to-be tried in conjunction with STI571. Our data demonstrate Endosymbiotic theory that mix of Pivanex with STI571 at low concentrations had a synergistic effect on apoptosis, cell viability reduction and caspase activity development. Erythroid differentiation was induced additively. The effects of a few HDI including butyric acid were linked with their power to modulate cell cycle and regulatory apoptotic genes. In this study we demonstrated reduction Ivacaftor ic50 inside the S phase cells and enhancement of cells in G2 M phase. BA and other HDI caused G2 M arrest in human CCRF CEM severe T lymphoblastic leukemia. The levels of BCR ABL protein were considerably and synergistically paid down with mix of low levels of Pivanex and STI571. STI571 triggers apoptosis associated with differentiation of BCR ABL good cells but the induc tion of differentiation and components of cell death are merely partly understood. Kohmura et a-l. have shown that erythroid difference induced by STI571 in K562 cells was accompanied by phosphorylation of P38MAP kinase and dephosphorylation of ERK. Many reports have suggested that induction of growth inhibition and erythroid differentiation in K562 cells induced by butyrate, requires inhibition of ERK and activation of p38MAP kinase pathways. Yu et al. Demonstrate that the mix of STI571 and HDI results in the down regulation of Raf, MEKand ERK.